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2.
Int J Mol Sci ; 17(6)2016 Jun 03.
Article in English | MEDLINE | ID: mdl-27271611

ABSTRACT

The increasing amount of heavy metals used in manufacturing equivalently increases hazards of environmental pollution by industrial products such as cadmium oxide (CdO) nanoparticles. Here, we aimed to unravel the CdO nanoparticle destiny upon their entry into lungs by inhalations, with the main focus on the ultrastructural changes that the nanoparticles may cause to tissues of the primary and secondary target organs. We indeed found the CdO nanoparticles to be transported from the lungs into secondary target organs by blood. In lungs, inhaled CdO nanoparticles caused significant alterations in parenchyma tissue including hyperemia, enlarged pulmonary septa, congested capillaries, alveolar emphysema and small areas of atelectasis. Nanoparticles were observed in the cytoplasm of cells lining bronchioles, in the alveolar spaces as well as inside the membranous pneumocytes and in phagosomes of lung macrophages. Nanoparticles even penetrated through the membrane into some organelles including mitochondria and they also accumulated in the cytoplasmic vesicles. In livers, inhalation caused periportal inflammation and local hepatic necrosis. Only minor changes such as diffusely thickened filtration membrane with intramembranous electron dense deposits were observed in kidney. Taken together, inhaled CdO nanoparticles not only accumulated in lungs but they were also transported to other organs causing serious damage at tissue as well as cellular level.


Subject(s)
Cadmium Compounds/adverse effects , Inhalation , Nanoparticles/adverse effects , Oxides/adverse effects , Animals , Cadmium/adverse effects , Cadmium/blood , Cadmium Compounds/blood , Cadmium Compounds/chemistry , Cadmium Compounds/metabolism , Environmental Exposure , Female , Kidney/metabolism , Kidney/pathology , Kidney/ultrastructure , Liver/metabolism , Liver/pathology , Liver/ultrastructure , Lung/metabolism , Lung/pathology , Lung/ultrastructure , Mice , Nanoparticles/chemistry , Oxides/blood , Oxides/chemistry , Oxides/metabolism , Particle Size , Spleen/metabolism , Spleen/pathology , Spleen/ultrastructure
3.
Proc Natl Acad Sci U S A ; 113(19): 5275-80, 2016 May 10.
Article in English | MEDLINE | ID: mdl-27118834

ABSTRACT

Nature has evolved several unique biomineralization strategies to direct the synthesis and growth of inorganic materials. These natural systems are complex, involving the interaction of multiple biomolecules to catalyze biomineralization and template growth. Herein we describe the first report to our knowledge of a single enzyme capable of both catalyzing mineralization in otherwise unreactive solution and of templating nanocrystal growth. A recombinant putative cystathionine γ-lyase (smCSE) mineralizes CdS from an aqueous cadmium acetate solution via reactive H2S generation from l-cysteine and controls nanocrystal growth within the quantum confined size range. The role of enzymatic nanocrystal templating is demonstrated by substituting reactive Na2S as the sulfur source. Whereas bulk CdS is formed in the absence of the enzyme or other capping agents, nanocrystal formation is observed when smCSE is present to control the growth. This dual-function, single-enzyme, aerobic, and aqueous route to functional material synthesis demonstrates the powerful potential of engineered functional material biomineralization.


Subject(s)
Cadmium Compounds/blood , Crystallization/methods , Cystathionine gamma-Lyase/chemistry , Minerals/chemical synthesis , Nanoparticles/chemistry , Nanoparticles/ultrastructure , Sulfides/blood , Biological Products/chemistry , Catalysis , Enzyme Activation , Light , Materials Testing , Molecular Conformation , Particle Size , Refractometry , Scattering, Radiation , Surface Properties
4.
JAMA Ophthalmol ; 133(10): 1144-50, 2015 Oct.
Article in English | MEDLINE | ID: mdl-26248281

ABSTRACT

IMPORTANCE: Abnormal body levels of essential elements and exposure to toxic trace metals have been postulated to contribute to the pathogenesis of diseases affecting many organ systems, including the eye. OBJECTIVE: To investigate associations between body levels of trace metals and the prevalence of glaucoma in a cross-sectional population-based study. DESIGN, SETTING, AND PARTICIPANTS: Blood or urine metallic element levels and information pertaining to ocular disease were available for 2680 individuals 19 years and older participating in the fourth Korea National Health and Nutrition Examination Survey between January 1, 2008, and December 31, 2009, the second and the third years of the survey (2007-2009). Glaucoma diagnosis was based on criteria established by the International Society of Geographic and Epidemiologic Ophthalmology. Demographic, comorbidity, and health-related behavior information was obtained via interview. Multivariable logistic regression analyses were performed to determine associations between blood and urine trace element levels and the odds of glaucoma diagnosis. All analyses were performed between September 2014 and December 2014. MAIN OUTCOME AND MEASURE: The presence or absence of glaucoma. RESULTS: After adjustment for potential confounders, blood manganese level was negatively associated with the odds of glaucoma diagnosis (odds ratio [OR], 0.44; 95% CI, 0.21-0.92). Blood mercury level was positively associated with glaucoma prevalence (OR, 1.01; 95% CI, 1.00-1.03). No definitive association was identified between blood cadmium or lead levels or urine arsenic level and a diagnosis of glaucoma. CONCLUSIONS AND RELEVANCE: These findings in a cross-sectional study of the South Korean population suggest that a lower blood manganese level and a higher blood mercury level are associated with greater odds of glaucoma. For more confidence that trace metals may have a role in the pathogenesis of glaucoma, prospective studies would need to confirm that the presence of such trace metals increases the chance of developing glaucoma.


Subject(s)
Glaucoma/blood , Glaucoma/epidemiology , Manganese Compounds/blood , Mercury Compounds/blood , Trace Elements/blood , Arsenicals/urine , Asian People , Cadmium Compounds/blood , Cross-Sectional Studies , Female , Glaucoma/diagnosis , Humans , Lead Poisoning/blood , Male , Middle Aged , Nutrition Surveys , Odds Ratio , Prevalence , Prospective Studies , Republic of Korea/epidemiology , Risk Factors , Spectrophotometry, Atomic , Surveys and Questionnaires
5.
Part Fibre Toxicol ; 10: 37, 2013 Aug 06.
Article in English | MEDLINE | ID: mdl-23915017

ABSTRACT

BACKGROUND: Quantum dots (QDs) have been used as novel fluorescent nanoprobes for various bioapplications. The degradation of QDs, and consequent release of free cadmium ions, have been suggested to be the causes of their overall toxicity. However, in contrast to sufficient investigations regarding the biological fate of QDs, a paucity of studies have reported their chemical fate in vivo. Therefore, the overall aim of our study was to understand the chemical fate of QDs in vivo and explore analytical techniques or methods that could be used to define the chemical fate of QDs in vivo. METHODS: Male ICR mice were administered a single intravenous dose (0.2 µmol/kg) of aqueous synthesized CdTe/ZnS aqQDs. Inductively coupled plasma-mass spectrometry (ICP-MS) was used to simultaneously measure the concentrations of cadmium (Cd) and tellurium (Te) in the blood and tissues over the course of a 28 day period. We compared the blood kinetic parameters and biodistributions of Cd and Te, and used the molar ratio of Cd:Te as a marker for QDs degradation. RESULTS: Cd and Te display different blood kinetics and biodistribution profiles. The Cd:Te ratio in the blood did not vary significantly within the first hour compared with intact CdTe/ZnS aqQDs. The Cd:Te ratio decreased gradually over time from the 6 h time point on. Cd accumulated in the liver, kidneys, and spleen. Te was distributed primarily to the kidneys. Sharp time-dependent increases in the Cd:Te ratio were found in liver tissues. CONCLUSIONS: QDs can undergo degradation in vivo. In vitro, QDs are chemically stable and do not elicit the same biological responses or consequences as they do in vivo. Our methods might provide valuable information regarding the degradation of QDs in vivo and may enable the design and development of QDs for biological and biomedical applications.


Subject(s)
Cadmium Compounds/blood , Cadmium Compounds/pharmacokinetics , Quantum Dots , Sulfides/blood , Sulfides/pharmacokinetics , Tellurium/blood , Tellurium/pharmacokinetics , Zinc Compounds/blood , Zinc Compounds/pharmacokinetics , Animals , Cadmium Compounds/administration & dosage , Injections, Intravenous , Kidney/metabolism , Liver/metabolism , Male , Mass Spectrometry , Mice, Inbred ICR , Spleen/metabolism , Sulfides/administration & dosage , Tellurium/administration & dosage , Tissue Distribution , Zinc Compounds/administration & dosage
6.
Toxicol Ind Health ; 29(2): 149-61, 2013 Mar.
Article in English | MEDLINE | ID: mdl-22080035

ABSTRACT

The aim of this study was to investigate the effect of cigarette smoking and occupational exposure to heavy metals on the degree of pro-oxidant/antioxidant imbalance in smelters. The investigations were performed on the blood and urine of 400 subjects: 300 male copper smelters and 100 nonexposed male subjects. Biological material was divided into three groups: nonsmokers, those who smoked less than 20 cigarettes a day and those who smoked more than 20 cigarettes a day. The results showed a significant increase in the concentration of lead, cadmium and arsenic in the blood and urine of smelters, while smoking more than 20 cigarettes a day caused a further increase in the concentration of these metals. The level of malondialdehyde was approximately twofold higher in the plasma of the smelters compared to the control group. We have observed a disturbance in the level of antioxidants in erythrocyte lysate manifested by an increase in metallothionein and glutathione concentrations as well as superoxide dismutase and glutathione peroxidase activities and the decrease in glutathione S-transferase activity. Cigarette smoking, years of work in metallurgy and age of smelters were additional factors significantly affecting the pro-oxidant/antioxidant balance.


Subject(s)
Metallurgy , Metals, Heavy/adverse effects , Occupational Exposure/adverse effects , Oxidative Stress/drug effects , Smoke/adverse effects , Smoking/blood , Adult , Arsenicals/blood , Arsenicals/urine , Cadmium Compounds/blood , Cadmium Compounds/urine , Erythrocytes/chemistry , Erythrocytes/metabolism , Glutathione/analysis , Humans , Lead/blood , Lead/urine , Male , Malondialdehyde/blood , Malondialdehyde/urine , Metallothionein/analysis , Middle Aged , Oxidoreductases/analysis , Smoking/urine , Nicotiana
7.
Toxicol Mech Methods ; 20(1): 7-13, 2010 Jan.
Article in English | MEDLINE | ID: mdl-20001568

ABSTRACT

Some residents of the Mae Sot district in Thailand have suffered long-term exposure to elevated dietary levels of cadmium. To test the hypothesis that chronic dietary cadmium exposure can cause imbalance in calcium dynamics and accelerate bone resorption, a group of these residents (156 men and 256 women aged >/= 50) were selected on the basis of previous records of elevated urinary cadmium and tested for urinary and blood cadmium, bone formation and resorption markers, and the renal tubular dysfunction markers. Both genders had high levels of blood and urinary cadmium and high urinary levels of the markers for renal dysfunction and bone resorption in a dose-response relationship to urinary cadmium. The excretion of bone resorption markers was positively correlated to the ratio of excreted calcium and urinary cadmium. The results of a multivariate regression analysis indicated that bone resorption was accelerated by impaired calcium reabsorption in renal tubules.


Subject(s)
Bone Resorption/etiology , Cadmium Compounds , Calcium/metabolism , Environmental Exposure/adverse effects , Kidney Diseases/etiology , Aged , Biomarkers/metabolism , Bone Resorption/epidemiology , Cadmium Compounds/adverse effects , Cadmium Compounds/blood , Cadmium Compounds/urine , Female , Humans , Kidney Diseases/epidemiology , Male , Middle Aged , Thailand/epidemiology
8.
Toxicol Ind Health ; 25(2): 129-35, 2009 Mar.
Article in English | MEDLINE | ID: mdl-19458135

ABSTRACT

Although cadmium (Cd) is extensively used for nickel-cadmium battery production, few recent reports are available on the effect of this toxic metal on the imbalance of biometals in occupational exposure. The current study was carried out to determine the Cd level and its effect on the content of bioelements: zinc, cooper, magnesium, and iron in blood and urine of workers exposed to Cd during nickel-cadmium battery production. beta(2)-microglobulins (beta(2)-MG), as indicators of kidney damage, were determined in urine.The study group comprised 32 male nickel-cadmium battery workers, and the control group had 15 male construction workers with no history of Cd exposure. Levels of Cd and bioelements were determined in blood and urine by atomic absorption spectrophotometry.Cd concentration in blood of exposed workers was around 10 microg/L and in urine ranged from 1.93 to 8.76 microg/g creatinine (cr). Urine Cd concentration was significantly higher in exposed workers than in the controls, although no statistical difference in beta(2)-MG content was observed in urine between the two groups. Blood Zn and Mg level were significantly reduced and urine Zn level was increased in Cd-exposed group when compared with controls.The mean Cd concentrations in blood and urine did not exceed the recommended reference values of 10 microg/L in blood and 10 microg/g cr in urine. Cd exposure resulted in disturbances of Zn in blood and urine and Mg in blood but had no effect on Cu and Fe content in biological fluids.


Subject(s)
Cadmium Compounds/adverse effects , Cadmium Poisoning/metabolism , Electric Power Supplies , Nickel , Occupational Diseases/etiology , Occupational Exposure/analysis , Adult , Cadmium Compounds/blood , Cadmium Compounds/urine , Environmental Monitoring/methods , Humans , Kidney Diseases/chemically induced , Kidney Diseases/metabolism , Magnesium/blood , Male , Middle Aged , Occupational Diseases/metabolism , Zinc/blood , beta 2-Microglobulin/urine
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